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Nat Clin Pract Nephrol. 2008 Feb;4(2):91-101. doi: 10.1038/ncpneph0695.

Altered fluid, electrolyte and mineral status in tropical disease, with an emphasis on malaria and leptospirosis.

Author information

1
Queen Saovabha Memorial Institute, Bangkok, Thailand. visithstprj@yahoo.com

Abstract

Fluid, electrolyte and mineral perturbations are prevalent features of tropical disease. Hemodynamic alterations, fever, nitrogen wasting, and changes in membrane transport and acid-base balance contribute to these perturbations. Models of malaria and leptospirosis have been used to show that common hemodynamic changes in tropical disease include decreased systemic vascular resistance, increased cardiac output and increased renal vascular resistance. Blood volume is initially increased, but it decreases as disease progresses. Response to fluid loading is decreased. Diabetes insipidus is occasionally observed in malaria. Hyponatremia occurs frequently in tropical diseases, as a result of increased levels of antidiuretic hormone (vasopressin), entry of sodium into cells, sodium loss and resetting of osmoreceptors. Natriuresis and kaliuresis are observed in patients with leptospirosis. Large amounts of sodium and potassium are lost in stool as a result of diarrhea. Hypernatremia is uncommon, whereas hypokalemia caused by hyperventilation is often observed (more frequently in patients with leptospirosis and kaliuresis). During severe tropical infective episodes, hyperkalemia results from intravascular hemolysis or rhabdomyolysis, and occasionally from decreased activity of Na+,K+-ATPase. Hypocalcemia, hypomagnesemia and hypophosphatemia are common features of both malaria and leptospirosis. Loss of magnesium in the urine is uniquely associated with leptospiral nephropathy. Hypozincemia and hypocupremia can also develop during tropical infection, and might interfere with a patient's immune response. These electrolyte and mineral perturbations are transient and quickly resolve when the disease is controlled.

PMID:
18227802
DOI:
10.1038/ncpneph0695
[Indexed for MEDLINE]

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